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Mouse Embryonic Lung Culture, A System to Evaluate the Molecular Mechanisms of Branching
07:32

Mouse Embryonic Lung Culture, A System to Evaluate the Molecular Mechanisms of Branching

Published on: June 30, 2010

PI3K-AKT pathway mediates growth and survival signals during development of fetal mouse lung

J Wang1, T Ito, N Udaka

  • 1Department of Pathology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.

Tissue & Cell
|February 8, 2005
PubMed

Insights

The PI3K-AKT pathway is crucial for fetal lung development, regulating cell growth, proliferation, and apoptosis. Inhibiting this pathway hinders lung branching and surfactant production.

Area of Science:

  • Developmental Biology
  • Cell Signaling
  • Molecular Biology

Background:

  • Fetal lung development is a complex process involving intricate signaling pathways.
  • The Phosphatidylinositol 3-kinase (PI3K)-AKT signaling pathway is implicated in various cellular functions, including growth and survival.

Purpose of the Study:

  • To investigate the role of the PI3K-AKT signaling pathway in mouse fetal lung development.
  • To determine the effects of fibroblast growth factor 1 (FGF1) and PI3K/MAPK inhibitors on lung morphogenesis, cell proliferation, and apoptosis.

Main Methods:

  • Western blotting and immunohistochemistry were used to assess pAKT expression in fetal lungs.
  • Explant cultures were treated with FGF1, PI3K inhibitors (LY294002, wortmannin), and a MAPK inhibitor (PD98059).
  • Assays for BrdU incorporation, apoptosis (TUNEL), and surfactant apoprotein C (SPC) expression were performed.

Main Results:

  • Phosphorylated AKT (pAKT) expression was high in early fetal lung development, localized to the respiratory epithelium.
  • FGF1 treatment enhanced lung branching and cell proliferation, while PI3K/MAPK inhibitors reduced these processes.
  • Inhibitors increased apoptosis in the mesenchyme and decreased SPC expression, with FGF1's effects being blocked by inhibitors.

Conclusions:

  • The PI3K-AKT signaling pathway is essential for mouse fetal lung development.
  • This pathway regulates lung morphogenesis, cell proliferation, apoptosis, and surfactant production.

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